Therapeutic potential of beta-caryophyllene against aflatoxin B1-Induced liver toxicity: biochemical and molecular insights in rats

Silveira, Alice Rosa da; Rosa, Érica Vanessa Furlan; Sari, Marcel Henrique Marcondes; Sampaio, Tuane Bazanella; Santos, Jamila Trindade Dos; Jardim, Natália Silva; Müller, Sigrid; Oliveira, Mauro Schneider; Nogueira, Cristina Wayne; Furian, Ana Flávia

doi:10.1016/j.cbi.2021.109635

Cited by 16 publications

(16 citation statements)

References 72 publications

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“…In the present study, treatment with BCP resulted in lipid peroxidation mitigation as well as dose-dependent enriched antioxidant capacity, as revealed by lowered MDA and H 2 O 2 and enhanced GPx, SOD, CAT, and GRx activities. These results agree with the previously reported antioxidant capacity of BCP in myocardium [ 16 , 18 ], hepatic [ 48 ], and renal [ 49 ] tissues. Furthermore, treatment with BCP was related with a significant escalation in nuclear translocation of Nrf2, with subsequent HO1 and NQO1 amplification, indicating an intensified Nrf2/HO1/NQO1 signaling pathway.…”

Section: Discussionsupporting

confidence: 93%

“…Previously, Li et al [ 50 ] reported that BCP enhanced Nrf2 activation in high glucose (HG)-induced glomerular mesangial cells (MCs). Additionally, via activating the Nrf2/HO1 signaling pathway, BCP mitigated focal cerebral ischemia-reperfusion damage [ 20 ], MPTP induced Parkinson’s disease [ 51 ], aflatoxin B1 induced liver toxicity [ 48 ], and sulfasalazine-induced nephrotoxicity [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

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β-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFκB and Nrf2/HO1/NQO1 Pathways

Younis

2022

JCDD

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Background: β-caryophyllene (BCP), a natural sesquiterpene, is extensively present in the essential oils of several plants. Cyclophosphamide (CYC) is an anticancer drug. However, its clinical usage is inadequate due to its cardiotoxicity. The aim of this study was to study the effects of BCP on cardiac injury induced by CYC exposure, and to identify the underlying mechanism of action. Methods: Five groups of Wistar rats were allocated. Group I (Normal), II (BCP), and III (CYC) acted as controls. Group IV, V (CYC + BCP) received BCP in two doses (100 and 200 mg/kg, orally, respectively) for 14 days after CYC challenge. CYC groups received 200 mg/kg, i.p. of the drug once on the first day of experiments. Results: CYC group displayed numerous ECG and histological irregularities and cardiac markers elevation. CYC induced lipid peroxidation and oxidative stress intensification, as well as inflammatory and apoptotic markers escalation. Treatment with BCP resulted in modified ECG traces and histological sections. BCP mitigated cardiac markers and lipid peroxidation whereas intensified antioxidant capacity. BCP activated Nrf2, with subsequent HO1 and NQO1 amplification. BCP diminished TLR4/NFκB pathway, which consequently lessened the inflammatory and apoptosis responses. Conclusion: BCP administration was associated with activated Nrf2/HO1/NQO1 and inhibited TLR4/NFκB pathways with subsequent enhanced anti-oxidative capacity and diminished inflammatory and apoptosis responses.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFκB and Nrf2/HO1/NQO1 Pathways

Younis

2022

JCDD

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“…Oxidative Medicine and Cellular Longevity the formation of free radicals, lipid peroxides, and protein adducts that subsequently provoke renal cell damage [3,4,7,9]. Moreover, renal oxidative stress is believed to trigger inflammation by upregulating several proinflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α, HSP25, and TLR4) with simultaneous inhibition of IL-10, which is a robust anti-inflammatory molecule [10][11][12].…”

Section: Discussionmentioning

confidence: 99%

“…Amikacin (AK) is an aminoglycoside antibiotic frequently utilized for treating infections and neonatal renal abscess caused by gram-negative bacteria [1][2][3][4]. Renal tubular cells excrete the drug in urine without metabolism, and nephrotoxicity could occur by excess accumulation of AK in the renal cortex [5].…”

Section: Introductionmentioning

confidence: 99%

“…Renal tubular cells excrete the drug in urine without metabolism, and nephrotoxicity could occur by excess accumulation of AK in the renal cortex [5]. Suggested mechanisms for AK-induced renal injury include mitochondrial membrane damage and lysosomal dysfunction that subsequently intensify the production of free radicals, thus predisposing to cellular oxidative stress [3,4]. Although the nephrotoxic effects of AK are dependent on dose and duration of treatment and could vary between individuals, acute renal failure is the most common complication [1,5].…”

Section: Introductionmentioning

confidence: 99%

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Antioxidative and Anti-Inflammatory Protective Effects of β-Caryophyllene against Amikacin-Induced Nephrotoxicity in Rat by Regulating the Nrf2/AMPK/AKT and NF-κB/TGF-β/KIM-1 Molecular Pathways

Rajab

Albukhari

Khan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Herein, the molecular pathogenic pathways implicated in renal injury triggered by amikacin (AK), together with the alleviating actions of β-caryophyllene (BCP), were investigated. Adult male Wistar rats ( n = 32 ) were disseminated to the four following groups ( n = 8 /group): normal group, positive control animals (PC) that received AK intraperitoneal injections for 14 days (500 mg/kg/day), and rats that received AK simultaneously with small (200 mg/kg/day) and high doses (400 mg/kg/day) of BCP. The PC renal tissues revealed abnormal histology alongside increased apoptosis and significantly elevated serum creatinine and urea with marked proteinuria and oliguria relative to the normal rats. Moreover, renal tissues from the PC animals also showed substantial upregulations in NF-κB/TGF-β/KIM-1, whilst Nrf2/AMPK/AKT/PCNA declined, at the gene and protein levels in comparison to the normal rats. Additionally, the levels of markers of oxidative stress (MDA/H2O2/protein adducts) and inflammation (TNF-α/IL-1β/IL-6/IL-18/TLR/HSP25) were substantially higher in the PC renal specimens, whereas the antioxidants (GSH/GPx/SOD1/CAT) and interleukin-10 decreased, relative to the NC group. Both BCP protocols improved the biochemical markers of renal functions, alleviated renal histopathology and apoptosis, and decreased NF-κB/TGF-β/KIM-1 alongside the concentrations of oxidative stress and proinflammatory markers, whilst promoting Nrf2/AMPK/AKT/IL-10/PCNA and the targeted antioxidants. However, the improving effects in the high-dose regimen were markedly stronger than those observed in animals treated with low dose of BCP. In conclusion, the present report is the first to connect NF-κB/TGF-β/KIM-1 proinflammatory and Nrf2/AMPK/AKT antioxidative stress pathways with the pathogenesis of AK-induced nephrotoxicity. Additionally, the current report is the first to disclose alleviating activities for BCP against AK-triggered nephrotoxicity by modulating multiple antioxidative stress with anti-inflammatory molecular pathways.

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Safety and toxicology of the dietary cannabinoid β-caryophyllene

Oliveira¹,

Silva²,

Silva³

et al. 2023

Neurobiology and Physiology of the Endocannabinoid System

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Therapeutic potential of beta-caryophyllene against aflatoxin B1-Induced liver toxicity: biochemical and molecular insights in rats

Cited by 16 publications

References 72 publications

β-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFκB and Nrf2/HO1/NQO1 Pathways

β-Caryophyllene Ameliorates Cyclophosphamide Induced Cardiac Injury: The Association of TLR4/NFκB and Nrf2/HO1/NQO1 Pathways

Antioxidative and Anti-Inflammatory Protective Effects of β-Caryophyllene against Amikacin-Induced Nephrotoxicity in Rat by Regulating the Nrf2/AMPK/AKT and NF-κB/TGF-β/KIM-1 Molecular Pathways

Safety and toxicology of the dietary cannabinoid β-caryophyllene

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